Evidence map›Paper›PMID 23658447›Full record

ArticleJournal of virology2013

Hepatitis C virus infection upregulates CD55 expression on the hepatocyte surface and promotes association with virus particles.

Budhaditya Mazumdar, Hangeun Kim, Keith Meyer, Sandip K Bose, Adrian M Di Bisceglie, Ratna B Ray, Michael S Diamond, John P Atkinson, Ranjit Ray

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Complement Inactivation Strategy ofInternational journal of molecular sciences · 2021
    Article
  6. Article
  7. Review
  8. Interactions of viruses and the humoral innate immune response.Clinical immunology (Orlando, Fla.) · 2020
    Review
  9. In the Crosshairs: RNA Viruses OR Complement?Frontiers in immunology · 2020
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Status of hepatitis C virus vaccination: Recent update.World journal of gastroenterology · 2016
    Review
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Budhaditya MazumdarDepartment of Internal Medicine, St. Louis University, St. Louis, Missouri, USA.
Hangeun Kim
Keith Meyer
Sandip K Bose
Adrian M Di Bisceglie
Ratna B Ray
Michael S Diamond
John P Atkinson
Ranjit Ray
Saint Louis University · USWashington University in St. Louis · US

Funding

Virology and Smallpox VaccinationsU54AI057160 · NIAID · WASHINGTON UNIVERSITY · PI RAY, RANJIT · 2003 to 2013
$80.9M
INTRACELLULAR C3 PROTEINS: SOURCE, COMPOSITION, TRAFFICKING AND FUNCTIONR01GM099111 · NIGMS · WASHINGTON UNIVERSITY · PI ATKINSON, JOHN · 2011 to 2019
$2.7M
NIAID NIH HHS U54 AI057160NIAID NIH HHS U54-AI057160NIGMS NIH HHS R01 GM099111
6 · The paper itself

Abstract

CD55 limits excessive complement activation on the host cell surface by accelerating the decay of C3 convertases. In this study, we observed that hepatitis C virus (HCV) infection of hepatocytes or HCV core protein expression in transfected hepatocytes upregulated CD55 expression at the mRNA and protein levels. Further analysis suggested that the HCV core protein or full-length (FL) genome enhanced CD55 promoter activity in a luciferase-based assay, which was further augmented in the presence of interleukin-6. Mutation of the CREB or SP-1 binding site on the CD55 promoter impaired HCV core protein-mediated upregulation of CD55. HCV-infected or core protein-transfected Huh7.5 cells displayed greater viability in the presence of CD81 and CD55 antibodies and complement. Biochemical analysis revealed that CD55 was associated with cell culture-grown HCV after purification by sucrose density gradient ultracentrifugation. Consistent with this, a polyclonal antibody to CD55 captured cell culture-grown HCV. Blocking antibodies against CD55 or virus envelope glycoproteins in the presence of normal human serum as a source of complement inhibited HCV infection. The inhibition was enhanced in the presence of both the antibodies and serum complement. Collectively, these results suggest that HCV induces and associates with a negative regulator of the complement pathway, a likely mechanism for immune evasion.

Indexed as

Analysis of VarianceAntibodies, ViralBinding SitesBlotting, WesternCD55 AntigensCell LineComplement Pathway, ClassicalDNA PrimersEnzyme-Linked Immunosorbent AssayFlow CytometryHepatitis CHepatocytesHumansInterleukin-6LuciferasesReal-Time Polymerase Chain ReactionAntibodies, ViralCD55 AntigensDNA PrimersInterleukin-6Luciferases

Identifiers

PMID23658447
PMCPMC3700207
OpenAlexW1983222054

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.